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Potential Effects of CXCL9 and CCL20 on Cardiac Fibrosis in Patients with Myocardial Infarction and Isoproterenol-Treated Rats

1
Ph.D. Program for Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University and Academia Sinica, Taipei 110, Taiwan
2
Department of Medicine, MacKay Medical College, New Taipei City 252, Taiwan
3
Division of Cardiology, Department of Internal Medicine, MacKay Memorial Hospital, Taipei 104, Taiwan
4
Graduate Institute of Cancer Molecular Biology and Drug Discovery, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan
5
Institute of Biological Chemistry, Academia Sinica, Taipei 115, Taiwan
6
TMU Biomedical Commercialization Center, Taipei Medical University, Taipei 110, Taiwan
7
Ph.D. Program in Biotechnology Research and Development, College of Pharmacy, Taipei Medical University, Taipei 110, Taiwan
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
J. Clin. Med. 2019, 8(5), 659; https://doi.org/10.3390/jcm8050659
Received: 15 April 2019 / Revised: 2 May 2019 / Accepted: 9 May 2019 / Published: 11 May 2019
(This article belongs to the Section Cardiology)
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Abstract

The chemokines CXCL9 and CCL20 have been reported to be associated with ventricular dysfunction. This study was aimed to investigate the effects of CXCL9/CCL20 on cardiac fibrosis following myocardial infarction (MI). Blood samples of patients with MI were obtained to determine the serum CXCL9, CCL20, tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β). The expression of CXCL9 and CCL20 in hypoxia-incubated H9c2 cells and TNF-α/TGF-β-activated peripheral blood mononuclear cells (PBMCs) were examined. The experimental MI of rats was produced by the intraperitoneal injection of isoproterenol (ISO) (85 mg/kg/day) for two consecutive days. The growth and migration of CXCL9/CCL20-incubated cardiac fibroblasts in vitro were evaluated. TNF-α/TGF-β-activated PBMCs showed an enhanced expression of CXCL9 and CCL20, while hypoxic H9c2 cells did not. Patients with MI had significantly enhanced levels of serum TGF-β and CXCL9 compared to healthy subjects. ISO-treated rats had increased serum CXCL9 levels and marked cardiac fibrosis compared to control rats. The trend of increased serum CCL20 in patients with MI and ISO-treated rats was not significant. CXCL9-incubated cardiac fibroblasts showed enhanced proliferation and migration. The findings of this study suggest that an enhanced expression of CXCL9 following MI might play a role in post-MI cardiac fibrosis by activating cardiac fibroblasts. View Full-Text
Keywords: myocardial infarction; cardiac fibrosis; CXCL9; CCL20; isoproterenol myocardial infarction; cardiac fibrosis; CXCL9; CCL20; isoproterenol
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Lin, C.-F.; Su, C.-J.; Liu, J.-H.; Chen, S.-T.; Huang, H.-L.; Pan, S.-L. Potential Effects of CXCL9 and CCL20 on Cardiac Fibrosis in Patients with Myocardial Infarction and Isoproterenol-Treated Rats. J. Clin. Med. 2019, 8, 659.

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